Abstract
Purpose/Objective: Angiogenesis is a crucial step for the continuous growth of solid tumors and the development of metastasis. The molecular events initiating the “angiogenic switch” remains elusive in prostate carcinoma (PC). The endothelial receptor tyrosine kinases, such as, the VEGF receptor and Tie-2 receptor are implicated in the “angiogenic switch” of PC. The Tie-2 receptor binds angiopoietins (Ang) and is selectively expressed in PC over normal prostate tissues. Since, Ang-1 promotes endothelial cell survival, we hypothesized that pre-treatment with a soluble murine Tie-2 receptor (mTek-Fc) would lead to blockade of Ang-1-mediated endothelial cell cytoprotection and would result in a cumulative inhibitory effect of RT on the PC growth.
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